The world has experienced some very large shifts in the epidemiology of carbon monoxide poisoning, but it remains one of the most important toxicological global causes of morbidity and mortality. The diagnosis can be quickly confirmed with blood gases pulse oximeters lack both sensitivity and specificity. Several strong predictors for serious neurological sequelae prolonged loss of consciousness and elevated S100B and reduced life expectancy elevated troponin are now reasonably well established. Despite this clearly defined high-risk group and extensive research into the pathophysiology, there has been little translation into better treatment. Much of the pathophysiological research has focused on hyperbaric oxygen. Yet it is apparent that clinical trials show little evidence for benefit from hyperbaric oxygen, and the most recent even raises the possibility of harm for repeated courses. More logical and promising potential antidotes have been under-researched, although recently both animal and small human studies suggest that erythropoietin may reduce S100B and prevent neurological sequelae. Major breakthroughs are likely to require further research on this and other treatments that may inhibit post-hypoxic inflammatory responses and apoptosis.

AbbreviationsCOCarbon monoxide

COHbCarboxyhemoglobin

DNSDelayed neurologic sequelae

ECGElectrocardiography

EPOErythropoietin

HBOHyperbaric oxygen

NSENeuron-specific enolase

PNSPersistent neurologic sequelae.

Electronic supplementary materialThe online version of this article doi:10.1186-cc13846 contains supplementary material, which is available to authorized users.